scholarly journals Transient cerebral hypoperfusion and hypertensive events during atrial fibrillation: a plausible mechanism for cognitive impairment

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Matteo Anselmino ◽  
Stefania Scarsoglio ◽  
Andrea Saglietto ◽  
Fiorenzo Gaita ◽  
Luca Ridolfi
Medicina ◽  
2019 ◽  
Vol 55 (12) ◽  
pp. 767 ◽  
Author(s):  
Ahmed AlTurki ◽  
Jakub B. Maj ◽  
Mariam Marafi ◽  
Filippo Donato ◽  
Giovanni Vescovo ◽  
...  

Atrial fibrillation (AF) is the most common arrhythmia encountered in clinical practice with implications on long-term outcomes. Metabolic disorders including diabetes mellitus and obesity are independent predictors of atrial fibrillation and present therapeutic targets to reduce both the incidence and duration burden of atrial fibrillation. The presence of pericardial fat in direct contact with cardiac structures, as well the subsequent release of proinflammatory cytokines, may play an important role in this connection. Atrial fibrillation is an independent predictor of cognitive impairment and dementia. While clinical stroke is a major contributor, other factors such as cerebral hypoperfusion and microbleeds play important roles. New evidence suggests that atrial fibrillation and cognitive impairment may be downstream events of atrial cardiomyopathy, which may be caused by several factors including metabolic syndrome, obesity, and obstructive sleep apnea. The mechanisms linking these comorbidities to cognitive impairment are not yet fully elucidated. A clearer understanding of the association of AF with dementia and cognitive impairment is imperative. Future studies should focus on the predictors of cognitive impairment among those with AF and aim to understand the potential mechanisms underlying these associations. This would inform strategies for the management of AF aiming to prevent continued cognitive impairment.


Angiology ◽  
2020 ◽  
Vol 71 (6) ◽  
pp. 498-519
Author(s):  
Theodora A. Manolis ◽  
Antonis A. Manolis ◽  
Evdoxia J. Apostolopoulos ◽  
Helen Melita ◽  
Antonis S. Manolis

Growing evidence suggests that atrial fibrillation (AF), in addition to its thromboembolic risk, is a risk factor for cognitive impairment (CI) via several pathways and mechanisms, further contributing to morbidity/mortality. Prior stroke is a contributor to CI, but AF is also associated with CI independently from prior stroke. Silent brain infarctions, microemboli and microbleeds, brain atrophy, cerebral hypoperfusion from widely fluctuating ventricular rates, altered hemostatic function, vascular oxidative stress, and inflammation may all exacerbate CI, particularly in patients with persistent/permanent rather than paroxysmal AF and with increased duration/burden of the arrhythmia. Brain magnetic resonance imaging is an important screening tool in eliciting and monitoring vascular and nonvascular lesions contributing to CI. Evidence is also emerging about the role of genetics in CI development. Anticoagulation and rhythm/rate control strategies may protect against CI preventing or slowing its progression or conversion to dementia, particularly at the early stages when CI may still be a treatable condition. Importantly, AF and CI share many common risk factors. Thus, screening for these 2 conditions and searching for and managing modifiable risk factors and potentially reversible causes for both AF and CI remains an important step toward prevention or amelioration of the impact incurred by these 2 conditions.


2019 ◽  
Vol 30 (11) ◽  
pp. 2052-2058 ◽  
Author(s):  
Dawn F. Wolfgram

The high frequency of cognitive impairment in individuals on hemodialysis is well characterized. In-center hemodialysis patients are disproportionately affected by cognitive impairment compared with other dialysis populations, identifying hemodialysis itself as a possible factor. The pathophysiology of cognitive impairment has multiple components, but vascular-mediated cerebral injury appears to contribute based on studies demonstrating increased cerebral ischemic lesions and atrophy in brain imaging of patients on hemodialysis. Patients on hemodialysis may be at increased risk for cerebral ischemic injury disease due to vasculopathy associated with ESKD and from their comorbid diseases, such as hypertension and diabetes. This review focuses on the intradialytic cerebral hypoperfusion that can occur during routine hemodialysis due to the circulatory stress of hemodialysis. This includes a review of current methods used to monitor intradialytic cerebral perfusion and the structural and functional cognitive outcomes that have been associated with changes in intradialytic cerebral perfusion. Monitoring of intradialytic cerebral perfusion may become clinically relevant as nephrologists try to avoid the cognitive complications seen with hemodialysis. Identifying the appropriate methods to assess risk for cerebral ischemic injury and the relationship of intradialytic cerebral hypoperfusion to cognitive outcomes will help inform the decision to use intradialytic cerebral perfusion monitoring in the clinical setting as part of a strategy to prevent cognitive decline.


2014 ◽  
Vol 261 (3) ◽  
pp. 546-553 ◽  
Author(s):  
Solveig Horstmann ◽  
Timolaos Rizos ◽  
Geraldine Rauch ◽  
Maximilian Fuchs ◽  
Cathrin Arden ◽  
...  

Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Jonathan Graff-Radford ◽  
Rosebud Roberts ◽  
Malini Madhavan ◽  
Alejandro Rabinstein ◽  
Ruth Cha ◽  
...  

The objective of this study was to investigate the cross-sectional associations of atrial fibrillation with neuroimaging measures of cerebrovascular disease and Alzheimer’s disease-related pathology, and their interaction with cognitive impairment. MRI scans of non-demented individuals (n=1044) from the population-based Mayo Clinic Study of Aging were analyzed for infarctions, total grey matter, hippocampal and white matter hyperintensity volumes. A subset of 496 individuals underwent FDG and C-11 Pittsburgh compound B (PiB) PET scans. We assessed the associations of atrial fibrillation with i) categorical MRI measures (cortical and subcortical infarctions) using multivariable logistic regression models, and with ii) continuous MRI measures ( hippocampal, total grey matter, and white matter hyperintensity volumes) and FDG-PET and PiB-PET measures using multivariable linear regression models, and adjusting for confounders. Among participants who underwent MRI (median age, 77.8, 51.6% male), 13.5% had atrial fibrillation. Presence of atrial fibrillation was associated with subcortical infarctions (odds ratio [OR], 1.83; p=0.002), cortical infarctions (OR, 1.91; p=0.03), total grey matter volume (Beta [β], -.025, p<.0001) after controlling for age, education, gender, APOE e4 carrier status, coronary artery disease, diabetes, history of clinical stroke, and hypertension. However, atrial fibrillation was not associated with white matter hyperintensity volume, hippocampal volume, Alzheimer’s pattern of FDG hypometabolism or PiB uptake. There was a significant interaction of cortical infarction (p for interaction=0.004) and subcortical infarction (p for interaction =0.015) with atrial fibrillation with regards to odds of mild cognitive impairment (MCI). Using subjects with no atrial fibrillation and no infarction as the reference, the OR (95% confidence intervals [CI]) for MCI was 2.98 (1.66, 5.35;p = 0.0002) among participants with atrial fibrillation and any infarction, 0.69 (0.36, 1.33;p= 0.27) for atrial fibrillation and no infarction, and 1.50 (0.96, 2.32;p = 0.07) for no atrial fibrillation and any infarction. These data highlight that atrial fibrillation is associated with MCI in the presence of infarctions.


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